ライフサイエンスコーパス: long QT

1 f AVB had a 7-fold higher risk of developing long QT.

2 more frequent in patients with drug-induced long QT.

3 3 but much less so for other common forms of long QT.

4 ssociated with cardiac arrhythmias including long QT.

5 thmia in females with inherited and acquired long-QT.

6 tly in clinical development for treatment of long QT-3 syndrome (LQT-3), hypertrophic cardiomyopathy

7 ium channel (Nav1.5) are associated with the long-QT-3 (LQT3) syndrome.

8 Drug-induced long QT and arrhythmia propensity substantially increase

9 riants in SCN5A and KCNH2, disease genes for long QT and Brugada syndromes, were assessed for potenti

10 n in humans that is associated with combined long QT and Brugada syndromes.

11 ontraindicated for patients with preexisting long-QT and those with repolarization abnormalities.

12 inpatients, 27.3% had abnormal ECG, 1.6% had long QT, and 0.9% qualified as drug-induced long QT case

13 Long-QT, arrhythmogenic right ventricular cardiomyopathy

14 is a risk factor for inherited and acquired long-QT associated torsade de pointes (TdP) arrhythmias,

15 to determine the prevalence of drug-induced long QT at admission to a public psychiatric hospital an

16 Channelopathies (short and long QT, Brugada, and catecholaminergic polymorphic vent

17 long QT, and 0.9% qualified as drug-induced long QT case subjects.

18 parison subjects, patients with drug-induced long QT had significantly higher frequencies of hypokale

19 5-year period were reviewed for drug-induced long QT (heart-rate corrected QT >/=500 ms and certain o

20 sed by mutations in KCNQ1, includes, besides long QT, hyperinsulinemia, clinically relevant symptomat

21 The long QT interval of type 1 diabetic hearts was shortened

22 0.009), in a pre-defined set of 7 congenital long QT interval syndrome (cLQTS) genes encoding potassi

23 re variants are associated with drug-induced long QT interval syndrome (diLQTS) and torsades de point

24 n KCNQ1, a gene previously implicated in the long QT interval syndrome.

25 major clinical feature of this syndrome is a long QT interval that results in cardiac arrhythmias.

26 etrospective analysis of an ECG identified a long QT interval, but sequencing of known LQT genes was

27 ivity of the channel are associated with the long QT (interval between the Q and T waves in electroca

28 Genetic long QT (LQT) syndrome is a life-threatening disorder ca

29 m channel (hNav1.5) is associated with fatal long QT (LQT) syndrome.

30 In type-2 long QT (LQT2), adult women and adolescent boys have a h

31 Patients with drug-induced long QT (N=62) were compared with a sample of patients w

32 patient indicated that 85.5% of drug-induced long QT patients had two or more factors, whereas 81.1%

33 el of inherited long QT syndrome rescues the long QT phenotype.

34 et of 15 KCNQ1 mutations with known clinical long QT phenotypes, we developed a method to stratify th

35 in 20% of Brugada syndrome (2/10) and 50% of long QT syndrome (1/2) and catecholaminergic polymorphic

36 rgic polymorphic ventricular tachycardia and long QT syndrome (17 [6%] and 11 [4%], respectively).

37 oal compound that clinically causes acquired long QT syndrome (acLQTS), which is associated with prol

38 ardiac events by antidepressants is acquired long QT syndrome (acLQTS), which produces electrocardiog

39 effect of CaM mutations causing CPVT (N53I), long QT syndrome (D95V and D129G), or both (CaM N97S) on

40 Drug-induced long QT syndrome (diLQTS) and congenital LQTS (cLQTS) sh

41 D causation have been found, particularly in long QT syndrome (e.g., KCNJ5, AKAP9, SNTA1), idiopathic

42 in patients with potassium channel-mediated long QT syndrome (ie, LQT1 and LQT2) has not been invest

43 disparate mutant ion channels that underlie long QT syndrome (LQT) and cystic fibrosis (CF).

44 a subunit, KCNQ1, constitute the majority of long QT syndrome (LQT-1) cases, we have carried out a de

45 he dominant mechanism associated with type 2 Long QT syndrome (LQT2) caused by Kv11.1 potassium chann

46 patients with sodium channel-mediated type 3 long QT syndrome (LQT3).

47 s identified in 115 (51%) of 225 RSCA cases: long QT syndrome (LQTS) (n = 48 [42%]), hypertrophic car

48 Changes in hERG channel function underlie long QT syndrome (LQTS) and are associated with cardiac

49 Long QT syndrome (LQTS) and catecholaminergic polymorphi

50 e the efficacy of different beta-blockers in long QT syndrome (LQTS) and in genotype-positive patient

51 Patients with long QT syndrome (LQTS) are predisposed to life-threaten

52 The heart rhythm disorder long QT syndrome (LQTS) can result in sudden death in th

53 Inherited long QT syndrome (LQTS) caused by loss-of-function mutat

54 Long QT syndrome (LQTS) exhibits great phenotype variabi

55 As genetic testing for long QT syndrome (LQTS) has become readily available, im

56 Fetal arrhythmias characteristic of long QT syndrome (LQTS) include torsades de pointes (TdP

57 Long QT syndrome (LQTS) is a genetic disease characteriz

58 Long QT syndrome (LQTS) is a leading cause of sudden car

59 Long QT syndrome (LQTS) is a potentially lethal but high

60 Long QT syndrome (LQTS) is a potentially lethal cardiac

61 Congenital Long QT syndrome (LQTS) is an arrhythmogenic disorder th

62 Long QT syndrome (LQTS) is an inherited or drug induced

63 Fetal long QT syndrome (LQTS) is associated with complex arrhy

64 Long QT syndrome (LQTS) is caused by the abnormal functi

65 Congenital long QT syndrome (LQTS) is characterized by QT prolongat

66 The diagnosis of long QT syndrome (LQTS) is rather straightforward.

67 A puzzling feature of the long QT syndrome (LQTS) is that family members carrying

68 Long QT syndrome (LQTS) is the first described and most

69 Long QT syndrome (LQTS) is the most common cardiac chann

70 Long QT syndrome (LQTS) may contribute to this problem.

71 entify risk factors for fatal arrhythmias in long QT syndrome (LQTS) patients presenting with syncope

72 reflexes, might identify high- and low-risk long QT syndrome (LQTS) type 1 (LQT1) patients.

73 Mutations in these channels can cause Long QT Syndrome (LQTS) which increases the risk for ven

74 f which harbor pathogenic variants linked to long QT syndrome (LQTS) with early and severe expressivi

75 acquired prolongation of the QT interval, or long QT syndrome (LQTS), are at risk of life-threatening

76 atification is of clinical importance in the long QT syndrome (LQTS), however, little genotype-specif

77 This review will focus on the long QT syndrome (LQTS), the most common of the potentia

78 ing sequence of the KCNH2 gene implicated in Long QT Syndrome (LQTS), which occurred once in 500 whol

79 patients at the highest phenotypic risk for long QT syndrome (LQTS)-associated life-threatening card

80 ponsible for the cardiac arrhythmia disease, long QT syndrome (LQTS).

81 kade significantly reduces cardiac events in long QT syndrome (LQTS).

82 ening arrhythmia in a 10-day-old infant with long QT syndrome (LQTS).

83 y life-threatening arrhythmia syndromes like long QT syndrome (LQTS).

84 ss-of-function mutations in KCNQ1 have KCNQ1 long QT syndrome (LQTS).

85 olymorphic ventricular tachycardia (CPVT) or long QT syndrome (LQTS).

86 resentation and management of the fetus with long QT syndrome (LQTS).

87 ive genes involved in the Mendelian disorder long QT syndrome (LQTS).

88 the efficacy of beta-blockers in congenital long QT syndrome (LQTS).

89 her variations in NOS1AP affect drug-induced long QT syndrome (LQTS).

90 nq1 gene are the leading cause of congenital long QT syndrome (LQTS).

91 Congenital long QT syndrome 2 (LQT2) is caused by loss-of-function

92 the ventricular action potential that causes long QT syndrome 2 (LQT2), with increased propensity for

93 atment with E-4031 to block I(Kr) (mimicking long QT syndrome 2) or with sea anemone toxin II to impa

94 om patients with the cardiac rhythm disorder long QT syndrome 3 (LQT3) carrying SCN5A sodium channel

95 Long QT Syndrome 3 (LQTS3) arises from gain-of-function

96 rhythmogenic activity in patients harbouring long QT syndrome 3 but much less so for other common for

97 impair Na(+) channel inactivation (mimicking long QT syndrome 3) prolonged AP duration (APD); however

98 cytoplasmic loop of Ca(V)1.2 channels causes long QT syndrome 8 (LQT8), a disease also known as Timot

99 the WT may have predisposed to the observed long QT syndrome and associated TdP.

100 hannel have been identified in patients with Long QT syndrome and cardiac arrhythmia.

101 All patients diagnosed with long QT syndrome and catecholaminergic polymorphic ventr

102 utations are associated with severe forms of long QT syndrome and catecholaminergic polymorphic ventr

103 mutations in hERG1 channels cause inherited long QT syndrome and increased risk of cardiac arrhythmi

104 mechanism by which inherited mutations cause long QT syndrome and potentially lethal arrhythmias.

105 alance the reduced repolarization reserve in long QT syndrome and prevent EADs and PVTs.

106 ce in situ hybridization has identified that long QT syndrome and sudden cardiac death may occur as a

107 ergic polymorphic ventricular tachycardia or long QT syndrome and sudden cardiac death.

108 Dysfunction of hERG causes long QT syndrome and sudden death, which occur in patien

109 ation or pharmacological inhibition produces Long QT syndrome and the lethal cardiac arrhythmia torsa

110 bulbar effect, quinidine can induce acquired long QT syndrome and torsade de pointes through its inte

111 l-developed case of acquired or drug-induced long QT syndrome as an exemplar case.

112 arge rearrangements in genes responsible for long QT syndrome as part of the molecular autopsy of a 3

113 Long QT syndrome associated mutations of this site lower

114 nt of future IKs channel activators to treat Long QT syndrome caused by diverse IKs channel mutations

115 Compared with long QT syndrome D96V-CaM, A103V-CaM had significantly l

116 pathogenicity of gene variants identified in long QT syndrome genetic screening.

117 rging algorithms for interpreting a positive long QT syndrome genetic test, the zebrafish cardiac ass

118 Long QT syndrome has been associated with sudden cardiac

119 This syndrome of drug-induced long QT syndrome has moved from an interesting academic

120 sted the ability of previously characterized Long QT Syndrome hERG1 mutations and polymorphisms to re

121 There was stronger clinical evidence of long QT syndrome in carriers (38.6% versus 5.5%, P=0.000

122 Type 2 long QT syndrome involves mutations in the human ether a

123 Long QT syndrome is a potentially lethal yet highly trea

124 Drug-induced long QT syndrome is generally ascribed to inhibition of

125 Genetic testing for Long QT Syndrome is now a standard and integral componen

126 ation since it was identified as a target of long QT syndrome more than 20 years ago.

127 ells in the absence of WT CaM except for the long QT syndrome mutant CaM D129G.

128 ectrophysiological analysis of corresponding long QT syndrome mutants suggested impaired PIP2 regulat

129 o exert these same effects on a prototypical long QT syndrome mutation (delKPQ).

130 ations are found in 13% of genotype-negative long QT syndrome patients, but the prevalence of CaM mut

131 potassium current (IKr) blockade to predict long QT syndrome prolongation and arrhythmogenesis.

132 ubjects with 34 mutations from multinational long QT syndrome registries were studied.

133 on of SGK1 in a zebrafish model of inherited long QT syndrome rescues the long QT phenotype.

134 For the primary care provider, long QT syndrome should be considered during the evaluat

135 ial and is the predominant cause of acquired long QT syndrome that can lead to fatal cardiac arrhythm

136 outcomes and to risk-stratify patients with long QT syndrome type 1 (LQT1).

137 (c.671C>T, p.T224M), a gene associated with long QT syndrome type 1, which can cause syncope and sud

138 her go-go (HERG) potassium channels underlie long QT syndrome type 2 (LQT2) and are associated with f

139 on of polymorphic ventricular tachycardia in long QT syndrome type 2 (LQT2) has been associated with

140 K(+)] and T-wave, we also analysed data from long QT syndrome type 2 (LQT2) patients, testing the hyp

141 d have key roles in diseases such as cardiac long QT syndrome type 2 (LQT2), epilepsy, schizophrenia

142 RNA decay (NMD) is an important mechanism of long QT syndrome type 2 (LQT2).

143 ions in the cardiac Kv11.1 channel can cause long QT syndrome type 2 (LQTS2), a heart rhythm disorder

144 Cardiac long QT syndrome type 2 is caused by mutations in the hu

145 Confocal Ca(2+) imaging of long QT syndrome type 2 myocytes revealed that GS967 sho

146 by GS967 prevents EADs and abolishes PVT in long QT syndrome type 2 rabbits by counterbalancing the

147 revealed that I(NaL) potentiates EADs in the long QT syndrome type 2 setting through (1) providing ad

148 VT induction in a transgenic rabbit model of long QT syndrome type 2 using intact heart optical mappi

149 Long QT syndrome type 3 (LQT3) is a lethal disease cause

150 on) had a variant previously associated with long QT syndrome type 3 (LQTS3).

151 otentially fatal arrhythmias associated with long QT syndrome type 3.

152 ur report describes a novel form of acquired long QT syndrome where the target modified by As(2)O(3)

153 5%) families: Brugada syndrome, 13/18 (72%); long QT syndrome, 3/18 (17%); and catecholaminergic poly

154 Of 16 participants, 13 (81%) had long QT syndrome, 9 (56%) were female, and median age wa

155 ion implantable cardioverter-defibrillators (long QT syndrome, 9; Brugada syndrome, 8; catecholaminer

156 Dysfunction of IKr causes long QT syndrome, a cardiac electrical disorder that pre

157 For Brugada syndrome, long QT syndrome, and DPP6 the efficacy of an ICD for pr

158 ymorphic ventricular tachycardia, congenital long QT syndrome, and hypertrophic cardiomyopathy.

159 with genetic ion channel disorders including long QT syndrome, Brugada syndrome, catecholaminergic po

160 ecific genetic arrhythmia disorders, such as long QT syndrome, Brugada Syndrome, or Catecholaminergic

161 potential to be used as pharmacotherapy for long QT syndrome, but can also be proarrhythmic.

162 rived cardiomyocytes have been used to study long QT syndrome, catecholaminergic polymorphic ventricu

163 e understanding by practicing cardiologists: long QT syndrome, catecholaminergic polymorphic ventricu

164 ythmogenic right ventricular cardiomyopathy, long QT syndrome, commotio cordis, and Kawasaki disease.

165 rgic polymorphic ventricular tachycardia and long QT syndrome, especially the RYR2 gene, as well as t

166 kade contributes importantly to drug-induced long QT syndrome, especially when repolarization reserve

167 ealthy subjects and patients with hereditary long QT syndrome, familial hypertrophic cardiomyopathy,

168 ardiotoxicity profiles for healthy subjects, long QT syndrome, hypertrophic cardiomyopathy, and dilat

169 Disease phenotypes were verified in long QT syndrome, hypertrophic cardiomyopathy, and dilat

170 contrast to the autosomal dominant forms of long QT syndrome, JLNS is a recessive trait, resulting f

171 y prevention patients with Brugada syndrome, long QT syndrome, or carrying the DPP6 haplotype approac

172 otentially fatal human arrhythmias including long QT syndrome, short QT syndrome, Brugada syndrome, a

173 The main inherited cardiac arrhythmias are long QT syndrome, short QT syndrome, catecholaminergic p

174 the majority of drugs implicated in acquired long QT syndrome, the most common cause of drug-induced

175 hannel dysfunction with patient phenotype in long QT syndrome, these have been largely unsuccessful.

176 mmonly used to estimate the risk of acquired long QT syndrome, this approach is crude, and it is wide

177 mmonly implicated in the pathogenesis of the long QT syndrome, type 2 (LQT2).

178 ted pathways involved in arrhythmogenesis in long QT syndrome, whereas proarrhythmic changes in intra

179 Reduction in I(Kr) causes long QT syndrome, which can lead to fatal arrhythmias tr

180 Mutations in either gene can cause long QT syndrome, which can lead to fatal arrhythmias.

181 e to mutations or certain medications causes long QT syndrome, which can lead to fatal ventricular ar

182 channel function is a main cause of acquired long QT syndrome, which can lead to ventricular arrhythm

183 side effects of pharmaco-therapy is acquired long QT syndrome, which is characterized by abnormal car

184 A reduction in the hERG current causes long QT syndrome, which predisposes affected individuals

185 We find that several Long QT syndrome-associated IKs channel mutations shift

186 treatments for cardiac disorders such as the long QT syndrome.

187 lymorphic ventricular tachycardia (CPVT) and long QT syndrome.

188 in normal cells and in cells with simulated long QT syndrome.

189 potent in the 'disease setting' of inherited long QT syndrome.

190 are being developed for congenital/acquired long QT syndrome.

191 trigger cardiac arrhythmias associated with long QT syndrome.

192 , are present in a minority of patients with long QT syndrome.

193 ell established in certain diseases, such as long QT syndrome.

194 style changes for patients and families with long QT syndrome.

195 important factor in acquired and congenital long QT syndrome.

196 in principle, prove useful for treatment of long QT syndrome.

197 xpression level of hERG channels, leading to long QT syndrome.

198 idocaine administration in clinical acquired long QT syndrome.

199 s associated with increased risk of acquired long QT syndrome.

200 nosis and treatment of autoimmune-associated long QT syndrome.

201 2000 and December 2009 in the Mayo Clinic's Long QT Syndrome/Genetic Heart Rhythm Clinic, all 24 (16

202 inite or probable diagnosis (17%), including Long-QT syndrome (13%), catecholaminergic polymorphic ve

203 Most mutations were found in families with long-QT syndrome (47%) or hypertrophic cardiomyopathy (4

204 been reported as a risk factor for acquired long-QT syndrome (aLQTS) and torsades de pointes (TdP).

205 Drug-induced long-QT syndrome (diLQTS) is an adverse drug effect that

206 which cause cardiac arrhythmias, such as the long-QT syndrome (LQT) and atrial fibrillation.

207 he main trigger for cardiac events in type 1 long-QT syndrome (LQT1).

208 The majority of type 2 long-QT syndrome (LQT2) stems from trafficking defective

209 Insight into type 6 long-QT syndrome (LQT6), stemming from mutations in the

210 es, have been associated with the congenital long-QT syndrome (LQT9).

211 diac sympathetic denervation reduces risk in long-QT syndrome (LQTS) and catecholaminergic polymorphi

212 ening cardiac arrhythmias such as congenital long-QT syndrome (LQTS) and catecholaminergic polymorphi

213 e disease, cardiomyopathy, and most recently long-QT syndrome (LQTS) and sudden infant death syndrome

214 genetic modifiers of disease severity in the long-QT syndrome (LQTS) as their identification may cont

215 Although the hallmark of long-QT syndrome (LQTS) is abnormal cardiac repolarizati

216 Inherited long-QT syndrome (LQTS) is associated with risk of sudde

217 Long-QT syndrome (LQTS) is characterized by a prolonged

218 Long-QT syndrome (LQTS) is characterized by such strikin

219 Long-QT syndrome (LQTS) may result in syncope, seizures,

220 The Brugada syndrome (BrS) and long-QT syndrome (LQTS) present as congenital or acquire

221 herited arrhythmia clinics and the Rochester long-QT syndrome (LQTS) registry.

222 In long-QT syndrome (LQTS) type 1, severely increased morta

223 ythmia syndromes capable of producing severe long-QT syndrome (LQTS) with mutations involving CALM1,

224 for life-threatening events in patients with long-QT syndrome (LQTS) with normal corrected QT (QTc) i

225 Long-QT syndrome (LQTS), a cardiac arrhythmia disorder w

226 harbors hereditary mutations associated with long-QT syndrome (LQTS), a potentially lethal cardiac ar

227 enetic disorders of the RAS/MAPK pathway and long-QT syndrome (LQTS), and future directions for the f

228 presence of the potentially lethal mendelian long-QT syndrome (LQTS).

229 phase of action potentials, is a hallmark of long-QT syndrome (LQTS).

230 thy (HCM) or cardiac channelopathies such as long-QT syndrome (LQTS); however, the underlying molecul

231 2), left ventricular noncompaction (n=1), or long-QT syndrome (n=2).

232 athogenicity of Kir2.1-52V in 1 patient with long-QT syndrome and also supports the use of isogenic h

233 ns associated with cardiac arrest, including long-QT syndrome and catecholaminergic polymorphic ventr

234 d acquired (drug-induced) forms of the human long-QT syndrome are associated with alterations in Kv11

235 blished in long-QT syndrome, its role in non-long-QT syndrome arrhythmogenic channelopathies and card

236 ing in a patient presenting with symptoms of long-QT syndrome as a proof of principle, we demonstrate

237 ngly, some drugs that were thought to induce long-QT syndrome by direct block of the rapid delayed re

238 esponsible for a novel autoimmune-associated long-QT syndrome by targeting the hERG potassium channel

239 Vs identified across 388 clinically definite long-QT syndrome cases and 1344 ostensibly healthy contr

240 pathogenic/benign status to nsSNVs from 2888 long-QT syndrome cases, 2111 Brugada syndrome cases, and

241 yndrome, a rare, autosomal-recessive form of long-QT syndrome characterized by deafness, marked QT pr

242 Long-QT syndrome could, therefore, benefit from having a

243 retrospective analysis of all patients with long-QT syndrome evaluated from July 1998 to April 2012

244 A test was considered positive for long-QT syndrome if the absolute QT interval prolonged b

245 Testing was positive for long-QT syndrome in 31 patients (18%) and borderline in

246 athematical models of acquired and inherited long-QT syndrome in male and female ventricular human my

247 aling pathway as the cause of a drug-induced long-QT syndrome in which alterations in several ion cur

248 otype may represent a more common pattern of long-QT syndrome inheritance than previously anticipated

249 Long-QT syndrome is a potentially fatal condition for wh

250 Long-QT syndrome is an inherited cardiac channelopathy c

251 ones are crucial for glucose regulation, and long-QT syndrome may cause disturbed glucose regulation.

252 f arrhythmogenic heart diseases, such as the long-QT syndrome or catecholaminergic polymorphic ventri

253 of abnormal patients was positive in 17% of long-QT syndrome patients and 13% of catecholaminergic p

254 s a major factor in triggering TdP in female long-QT syndrome patients.

255 ent, monogenetic substrate for the patient's long-QT syndrome phenotype.

256 ese cases should be treated as a higher-risk long-QT syndrome subset similar to their Jervell and Lan

257 at CACNA1C is a bona fide, definite evidence long-QT syndrome susceptibility gene.

258 e that the recessive inheritance of a severe long-QT syndrome type 1 phenotype in the absence of an a

259 v11.1 voltage-gated potassium channel) cause long-QT syndrome type 2 (LQT2) because of prolonged card

260 ed sodium channel [NaV1.5]) cause congenital long-QT syndrome type 3 (LQT3).

261 get block of IKr in the setting of inherited long-QT syndrome type 3 and heart failure.

262 gers in bradycardia-dependent arrhythmias in long-QT syndrome type 3 as well tachyarrhythmogenic trig

263 A long-QT syndrome type 3 child experienced paradoxical QT

264 m increased INaL from inherited defects (eg, long-QT syndrome type 3 or disease-induced electric remo

265 kers are used as gene-specific treatments in long-QT syndrome type 3, which is caused by mutations in

266 hannels in the setting of normal physiology, long-QT syndrome type 3-linked DeltaKPQ mutation, and he

267 The basic defect in long-QT syndrome type III (LQT3) is an excessive inflow

268 An emerging standard-of-care for long-QT syndrome uses clinical genetic testing to identi

269 endent cohort of 82 subjects with congenital long-QT syndrome without an identified genetic cause.

270 CaM contain targets for mutations linked to long-QT syndrome, a type of inherited arrhythmia.

271 kcnh2, affected in Romano-Ward syndrome and long-QT syndrome, and cardiac troponin T gene, tnnt2, af

272 pts, the experience obtained in the study of long-QT syndrome, Brugada syndrome, and arrhythmogenic c

273 ic denervation (LCSD) is well established in long-QT syndrome, its role in non-long-QT syndrome arrhy

274 In long-QT syndrome, transmembrane segments S3-S5+S6 and th

275 ses, such as hypertrophic cardiomyopathy and long-QT syndrome, uncovered large-effect genetic variant

276 RG function is the primary cause of acquired long-QT syndrome, which predisposes affected individuals

277 s) have been identified in the 2 most common long-QT syndrome-susceptibility genes (KCNQ1 and KCNH2).

278 A mutational analysis of the major long-QT syndrome-susceptibility genes (KCNQ1, KCNH2, and

279 to arrhythmogenic phenotypes associated with long-QT syndrome.

280 mmon genetic variation at KCNQ1 with risk of long-QT syndrome.

281 ression of Kv11.1a and Kv11.1a-USO can cause long-QT syndrome.

282 loci included genes implicated in mendelian long-QT syndrome.

283 nts a novel mechanism in the pathogenesis of long-QT syndrome.

284 a large referral population of patients with long-QT syndrome.

285 ventricular arrhythmia syndromes other than long-QT syndrome.

286 stimulation of I(Ks), which can give rise to long-QT syndrome.

287 is other than autosomal dominant or sporadic long-QT syndrome.

288 the settings of both inherited and acquired long-QT syndrome.

289 pe in >/=1 relatives: 14 Brugada syndrome; 4 long-QT syndrome; 1 catecholaminergic polymorphic ventri

290 ilies (25%), including Brugada syndrome (7), long QT syndromes (5), dilated cardiomyopathy (2), and h

291 Long QT syndromes (LQTS) arise from many genetic and non

292 ities in the duration (for example, short or long QT syndromes and heart failure) or pattern (for exa

293 ; P<0.0001) with 17 Brugada syndromes and 15 long QT syndromes diagnosed based on pharmacological tes

294 forms, potentially aiding the study of short/long QT syndromes that result from abnormal changes in a

295 o EAD formation in clinical settings such as long QT syndromes, heart failure, and increased sympathe

296 humans with restrictive cardiomyopathies and long QT syndromes.

297 ay provide therapeutic efficacy for treating long QT syndromes.

298 Patients with hereditary short-QT or long-QT syndromes, representing the very extremes of the

299 ible to torsade de pointes (TdP) in acquired long QT type 2 than males, in-part due to higher L-type

300 , caveolin-3 (Cav3), have been linked to the long QT type 9 inherited arrhythmia syndrome (LQT9) and